CN113332267A - Application of sodium phenylbutyrate in preparation of medicine for preventing or treating Parkinson's disease - Google Patents
Application of sodium phenylbutyrate in preparation of medicine for preventing or treating Parkinson's disease Download PDFInfo
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- 229960002232 sodium phenylbutyrate Drugs 0.000 title claims abstract description 33
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- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61K—PREPARATIONS FOR MEDICAL, DENTAL OR TOILETRY PURPOSES
- A61K31/00—Medicinal preparations containing organic active ingredients
- A61K31/185—Acids; Anhydrides, halides or salts thereof, e.g. sulfur acids, imidic, hydrazonic or hydroximic acids
- A61K31/19—Carboxylic acids, e.g. valproic acid
- A61K31/192—Carboxylic acids, e.g. valproic acid having aromatic groups, e.g. sulindac, 2-aryl-propionic acids, ethacrynic acid
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- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61P—SPECIFIC THERAPEUTIC ACTIVITY OF CHEMICAL COMPOUNDS OR MEDICINAL PREPARATIONS
- A61P25/00—Drugs for disorders of the nervous system
- A61P25/14—Drugs for disorders of the nervous system for treating abnormal movements, e.g. chorea, dyskinesia
- A61P25/16—Anti-Parkinson drugs
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Abstract
The invention relates to the field of biological pharmacy, in particular to application of Sodium Phenylbutyrate (SP) in preparing a medicament for preventing or treating Parkinson's disease. The invention integrates multiple groups of chemical data to explore a gene co-expression network, and obtains the medicine SP which can obviously reverse the abnormally expressed gene in the module. Animal experiments show that the medicine can improve animal behavior and prevent development of Parkinson's disease. Thus, SP has the effect of preventing the development of Parkinson's disease and improving the effect of treatment of Parkinson's disease.
Description
Technical Field
The invention relates to the field of biological pharmacy, in particular to application of sodium phenylbutyrate in preparing a medicament for preventing or treating Parkinson's disease.
Background
Parkinson's Disease (PD) is the second most common neurodegenerative disease in the world, and there is currently no effective therapy to prevent or arrest the progression of PD. The disease can only be improved, cannot prevent the development of the disease and even cannot be cured no matter the disease is treated by medicines or operations at present.
Sodium Phenylbutyrate (SP) is commonly used in all neonatal patients with enzyme deficiency (manifested as complete enzyme deficiency in 28d after birth), delayed enzyme deficiency with a family history of hyperammonemic encephalopathy (manifested as partial enzyme deficiency after the first month of birth).
Disclosure of Invention
The invention aims to overcome the defects of the prior art and provides the application of the sodium phenylbutyrate in preparing the medicine for preventing or treating the Parkinson's disease. The invention discovers that the SP has the functions of preventing PD and relieving PD symptoms.
In order to achieve the purpose, the invention adopts the technical scheme that: provides an application of sodium phenylbutyrate in preparing a medicament for preventing and/or treating Parkinson's disease.
The invention applies a bioinformatics approach to weighted gene co-expression network analysis and identification of differential co-expression modules associated with organisms. 277 genes closely related to the Parkinson disease are matched into a gene network module by means of statistical test to obtain a gene co-expression module related to the Parkinson disease, and the medicament SP capable of obviously reversing the abnormally expressed genes in the module is obtained through a correlation spectrum database and differential gene expression spectrum data between samples of the substantia nigra brain region of a Parkinson patient and a normal control group. The ability of SP to reverse abnormal gene expression was confirmed by real-time quantitative polymerase chain reaction (qt-PCR) experiments. Animal experiments show that the medicine can improve animal behaviors and prevent the development of Parkinson's disease, and indicate that SP has the capacity of restoring the activity of dopamine neurons.
As a preferred embodiment of the use of the present invention, the pharmaceutical dosage form for preventing and/or treating parkinson's disease is a capsule, a tablet, an oral preparation, a microcapsule, an injection, a suppository, a spray or an ointment.
As a preferred embodiment of the use according to the invention, the medicament further comprises a pharmaceutically acceptable carrier.
The invention also provides a pharmaceutical composition for preventing and/or treating Parkinson's disease, which comprises sodium phenylbutyrate and a pharmaceutically acceptable carrier.
As a preferred embodiment of the pharmaceutical composition of the present invention, the pharmaceutical composition is for subcutaneous injection, intravenous injection, intramuscular injection or nasal administration.
The invention also provides application of the pharmaceutical composition in preparing a medicament for preventing and/or treating Parkinson's disease.
The invention has the beneficial effects that:
the invention provides a new application of sodium phenylbutyrate in preparing a medicine for preventing or treating Parkinson's disease, the medicine provided by the invention is reliable in production, stable in quality and exact in curative effect, can obviously prevent synaptic injury caused by reduction of mitochondrial function in Parkinson's disease, effectively reduces mitochondrial membrane injury, reduces mitochondrial edema, effectively increases expression of synaptic specific protein, improves activity of dopamine, prevents pathological changes of Parkinson's disease, and improves behavioral symptoms of Parkinson's disease.
Drawings
FIG. 1: the number of cell survivors per field is shown schematically.
FIG. 2: effect of dosing on mouse body weight. Wherein NC: control group before treatment; ROT: a ROT group before treatment; SP: SP groups before processing; NC 2: a treated control group; ROT 2: a processed ROT group; SP 2: a processed SP group; *: p is less than 0.05.
FIG. 3: effect of dosing on mouse behaviours.
Detailed Description
To more clearly illustrate the technical solutions of the present invention, the following embodiments are further described, but the present invention is not limited thereto, and these embodiments are only some examples of the present invention.
In order to facilitate better understanding of the present invention, the following detailed description will further illustrate the advantageous effects of the present invention through pharmacodynamic experiments, comparative experiments, and the like. Animal experiments prove that the sodium phenylbutyrate can effectively prevent the behavioral change of the Parkinson's disease. Cell experiments prove that the sodium phenylbutyrate can reduce mitochondrial membrane damage, reduce mitochondrial edema, effectively increase synaptic specific protein expression, improve dopamine activity and prevent Parkinson's disease characterized by neuronal synaptopathy. Thus indicating that the sodium phenylbutyrate has the effect of preventing the Parkinson disease.
In order to verify the pharmacological action of the medicament in treating the Parkinson's disease and provide scientific basis for clinical application of the medicament, the following pharmacodynamic experiments are specially carried out. The experiment adopts a Parkinson disease mouse model to detect relevant indexes of behavioristics, cell morphology and imaging.
The test drug of the present invention, Rotenone (ROT), Sodium Phenylbutyrate (SP), was purchased from ApexBio Technology, USA.
Example 1 cellular Primary synapse morphology assay
Purchasing 0-day C57 suckling mice to extract cortical neuron cells, treating the neuron cells with SP for 2h after the neuron cells grow out of the nerve synapse, adding ROT to construct a PD cell model, observing the cell synapse morphology after 24h, developing the neural synapse tubulin by using tubulin, developing the neuron cells by using Neu N, and observing the cell number of each 4 Xvisual field by using BX 86.
NC: a control group;
ROT: ROT treatment group, which was given 400 μ M ROT;
ROT + SP: the ROT group for SP intervention was given SP 1 μ M.
As a result, as shown in fig. 1, the number of viable cells per field in the ROT group was 132.67 fewer than that in the NC group, and p was 0.012; the number of viable cells per field in the ROT + SP group was 46.00 more than that in the ROT group, and p was 0.005.
Example 2 animal experiments and results
2.1 Experimental materials and Equipment
2.1.1 test subjects
A Parkinson (PD) mouse model, C57BL/6J mouse, was provided by Experimental animal technology, Inc. of Wintolite, Beijing (animal license number: SCXK (Jing) 2016-.
2.1.2 Experimental conditions
The clean animal room is free to eat and drink water at the temperature of 22-25 ℃ and the relative humidity of 40-60% in 12/12h light and dark period. The feeding and the material taking of the animals in the experimental process all comply with the relevant regulations of the management and the protection of the experimental animals.
2.1.3 Main Experimental instrumentation
A Roche Modular-ISE9OO-P800 type full-automatic biochemical analyzer; electronic balance model BP12 lS; LDZ5-2 desk type low speed automatic balancing centrifuge; spectrum lab model 22PC spectrophotometer; a Japanese photoelectric MEK-6318K full-automatic blood cell analyzer; a Thermo adjustable pipettor; leicirm 2135 microtome; BMJ-III type biological tissue embedding machine; TSJ-Q type full-automatic closed tissue dehydrator; PHY-III type pathological tissue bleaching and drying instrument; OLYMPUS-BX40 light microscope.
2.2 Experimental methods
2.2.1 establishment of DP rat model
According to the literature method: krishna Gokul, Muraldhara. organic documents of aqueous extract, oxidative antigens and biochemical induced by a polypeptide in microorganism, release to Parkinson's disease. neurocache Res.2014Jul; 39(7) 1382-94.doi:10.1007/s11064-014-1323-1.Epub2014May 16.
2.2.2 mice grouping and dosing methods
Blank control group: c57BL/6J mice were given 10% DMSO treatment;
parkinsonian model group: c57BL/6J mice were given 10% DMSO + ROT (1mg/kg) treatment;
drug control group: c57BL/6J mice were given 10% DMSO + SP (300mg/kg) treatment;
experimental groups: c57BL/6J mice were given 10% DMSO + ROT (1mg/kg) + SP (300mg/kg) treatment.
2.2.3 general conditions in mice
This experiment included 4 groups of 48 male 8WC57 mice participating in the experiment.
2.2.4 weight gain of mice.
When the selection is carried out, the weight of each group is not different, the ROT group body is reduced after the treatment, and the rest groups have no obvious change. (FIG. 2)
2.3 mouse behavioural assay
After the mice are subjected to grouping treatment, the behavioural changes of the mice are detected through a gait experiment, a sugar preference experiment and a forced swimming experiment.
The results are shown in fig. 3, and the PD gait experiment is mainly manifested as gait change and footprint repetition rate decrease. The PD model constructed by ROT shows the change of the action direction, p is less than 0.05, the step difference is increased, p is 0.002, the step width difference is increased, and p is 0.001. After SP administration, the mouse had no significant change in the direction of action, increased step size and increased step width, with p values of 0.0001 and 0.01, respectively. The carbohydrate preference experiment shows that the ROT-induced PD mice have obviously reduced carbohydrate preference, and the carbohydrate preference is restored to normal level after SP treatment. Forced swimming experiments show that the abandoning exercise time of the ROT group is obviously longer than that of the NC group, and the abandoning exercise time is obviously reduced after SP is given.
3. Statistical analysis
All GTVPET-AS profiles were compared to GTVPET using DSC calculated by Matlab 2016b (MathWorks Inc. of nano-tex, massachusetts, usa). The mean and Standard Deviation (SD) of each index were also calculated. The results were analyzed using the Kruskal-Wallis test. All values in the figures and text are expressed as mean ± standard error of the mean (SEM). Motor performance in the behavioral test is expressed in absolute values. The differences between groups were analyzed by an analysis of variance (ANOVA) using Dunnett and Tukey post-tests for comparison. p < 0.05 was considered statistically significant (n ═ number of mice included in each analysis). Statistical analysis was performed using SPSS 19.
Finally, it should be noted that the above embodiments are only used for illustrating the technical solutions of the present invention and not for limiting the protection scope of the present invention, and although the present invention is described in detail with reference to the preferred embodiments, it should be understood by those skilled in the art that modifications or equivalent substitutions can be made on the technical solutions of the present invention without departing from the spirit and scope of the technical solutions of the present invention.
Claims (6)
1. Application of sodium phenylbutyrate in preparing medicine for preventing and/or treating Parkinson's disease.
2. The use according to claim 1, wherein the pharmaceutical dosage form for preventing and/or treating Parkinson's disease is capsule, tablet, oral preparation, microcapsule preparation, injection, suppository, spray or ointment.
3. The use of claim 1, wherein the medicament further comprises a pharmaceutically acceptable carrier.
4. A pharmaceutical composition for preventing and/or treating parkinson's disease, comprising sodium phenylbutyrate and a pharmaceutically acceptable carrier.
5. The pharmaceutical composition of claim 4, wherein the pharmaceutical composition is for subcutaneous, intravenous, intramuscular, or nasal administration.
6. Use of the pharmaceutical composition of claim 4 for the manufacture of a medicament for the prevention and/or treatment of parkinson's disease.
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Cited By (1)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CN117338763A (en) * | 2023-11-01 | 2024-01-05 | 重庆医科大学 | Application of sodium butyrate in the preparation of drugs for the treatment of Parkinson's disease and its new therapeutic target |
Citations (6)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CN102065897A (en) * | 2008-04-29 | 2011-05-18 | 法奈科斯公司 | New therapeutic approaches for treating alzheimer disease and related disorders through a modulation of cell stress response |
| WO2013149091A1 (en) * | 2012-03-29 | 2013-10-03 | The Regents Of The University Of Colorado, A Body Corporate | Composition and method for treating neurodegenerative disease |
| CN103764166A (en) * | 2011-06-22 | 2014-04-30 | 通用医疗公司 | Treatment of proteinopathies |
| CN105050593A (en) * | 2013-03-24 | 2015-11-11 | 艾米利克斯制药公司 | Compositions for enhancing cell viability and methods of using same |
| CA3017573A1 (en) * | 2016-03-15 | 2017-09-21 | Acer Therapeutics Inc. | Palatable compositions including sodium phenylbutyrate and uses thereof |
| WO2017220315A1 (en) * | 2016-06-22 | 2017-12-28 | Universite Du Luxembourg | Means and methods for treating parkinson's disease |
-
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- 2021-03-31 CN CN202110345018.5A patent/CN113332267A/en active Pending
Patent Citations (7)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CN102065897A (en) * | 2008-04-29 | 2011-05-18 | 法奈科斯公司 | New therapeutic approaches for treating alzheimer disease and related disorders through a modulation of cell stress response |
| CN103764166A (en) * | 2011-06-22 | 2014-04-30 | 通用医疗公司 | Treatment of proteinopathies |
| WO2013149091A1 (en) * | 2012-03-29 | 2013-10-03 | The Regents Of The University Of Colorado, A Body Corporate | Composition and method for treating neurodegenerative disease |
| CN105050593A (en) * | 2013-03-24 | 2015-11-11 | 艾米利克斯制药公司 | Compositions for enhancing cell viability and methods of using same |
| CA3017573A1 (en) * | 2016-03-15 | 2017-09-21 | Acer Therapeutics Inc. | Palatable compositions including sodium phenylbutyrate and uses thereof |
| WO2017160345A1 (en) * | 2016-03-15 | 2017-09-21 | Acer Therapeutics Inc. | Palatable compositions including sodium phenylbutyrate and uses thereof |
| WO2017220315A1 (en) * | 2016-06-22 | 2017-12-28 | Universite Du Luxembourg | Means and methods for treating parkinson's disease |
Non-Patent Citations (3)
| Title |
|---|
| AVIK ROY等: "Sodium phenylbutyrate controls neuroinflammatory and antioxidant activities and protects dopaminergic neurons in mouse models of Parkinson"s disease", 《PLOS ONE》 * |
| EDITH STURM等: "Neuroprotection by Epigenetic Modulation in a Transgenic Model of Multiple System Atrophy", 《NEUROTHERAPEUTICS》 * |
| WENBO ZHOU等: "Phenylbutyrate Up-regulates the DJ-1 Protein and Protects Neurons in Cell Culture and in Animal Models of Parkinson Disease", 《THE JOURNAL OF BIOLOGICAL CHEMISTRY》 * |
Cited By (1)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CN117338763A (en) * | 2023-11-01 | 2024-01-05 | 重庆医科大学 | Application of sodium butyrate in the preparation of drugs for the treatment of Parkinson's disease and its new therapeutic target |
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Application publication date: 20210903 |